Cardiovascular disease (CVD) is the leading cause of death, globally. The most prevalent and devastating CVD is atherosclerosis, a chronic, inflammatory, fibroproliferative disorder primarily of large- and medium-sized conduit arteries. Its initiation and progression is closely linked to the vascular endothelium, which responds to the dynamic forces acting on the vessel wall because of the complex geometry of the arteries, and the acquired presence of pathologic characteristics such as atherosclerotic plaque.
The majority of cardiovascular events, like stroke and myocardial infarction, are caused by atherosclerotic plaque ruptures, which cause distal embolization. Previous studies have shown that hemodynamic quantities are linked to the initiation, progression and rupture of atherosclerotic plaques. These hemodynamic quantities are in turn influenced both by systemic properties and the local geometry (certain regions, like bifurcations are predisposed to plaque formation). Thus, hemodynamic quantities, i.e. pressure, velocities, flow rate and flow-generated endothelial shear stresses (ESS), play a crucial role in the understanding of plaque initiation, progression, and rupture. Further, a combination of hemodynamic factors with other patient information (like demographics, blood biomarker information, past history, etc.) can be used to obtain a coherent understanding of the patient's condition as well as better understanding of patient outcomes.